Background: Postoperative nausea and vomiting (PONV) are common side-effects following strabismus surgery. The present study aimed to compare the effects of different doses of dexmedetomidine (DEX) on PONV incidence in pediatric patients undergoing strabismus surgery. Methods: In this prospective randomized double-blinded study, 126 pediatric patients undergoing strabismus surgery were randomized into one of three groups: Placebo group, normal saline; DEX1 group, 0.3 μg/kg dexmedetomidine, and DEX2 group, 0.5 μg/kg dexmedetomidine. Oculocardiac reflex (OCR) events were recorded during surgery. PONV or postoperative vomiting (POV) was recorded for 24 h in the ward. Pediatric anesthesia emergence delirium (PAED) scale and emergence agitation (EA) scale were recorded in the recovery room. Results: Intraoperative OCR was significantly reduced in DEX2 group (42%) as compared to that of Placebo group (68%) (p = 0.0146). During the first 24 h post-op, the overall incidence of PONV was significantly lower in DEX2 group (10%) than that of Placebo group (32%) (p = 0.0142). There was no significant difference in POV among the three groups. PAED or EA scores among the three groups were similar during recovery time. Conclusion: Dexmedetomidine (0.5 μg/kg) reduced OCR and PONV without lengthening extubation time or recovery time in pediatric patients undergoing strabismus surgery.

Dry eye disease (DED) affects nearly 55% of people worldwide; several studies have proposed that central sensitization and neuroinflammation may contribute to the developing corneal neuropathic pain of DED, while the underlying mechanisms of this contribution remain to be investigated. Excision of extra orbital lacrimal glands established the dry eye model. Corneal hypersensitivity was examined through chemical and mechanical stimulation, and open field test measured the anxiety levels. Restingstate fMRI is a method of functional magnetic resonance imaging (rs‐fMRI) was performed for anatomical involvement of the brain regions. The amplitude of low‐frequency fluctuation (ALFF) determined brain activity. Immunofluorescence testing and Quantitative real‐time polymerase chain reaction were also performed to further validate the findings. Compared with the Sham group, ALFF signals in the supplemental somatosensory area, secondary auditory cortex, agranular insular cortex, temporal association areas, and ectorhinal cortex brain areas were increased in the dry eye group. This change of ALFF in the insular cortex was linked with the increment in corneal hypersensitivity (p < 0.01), c‐Fos (p < 0.001), brain‐derived neurotrophic factor (p < 0.01), TNF‐α, IL‐6, and IL‐1β (p < 0.05). In contrast, IL‐10 levels (p < 0.05) decreased in the dry eye group. DED‐induced corneal hypersensitivity and upregulation of inflammatory cytokines could be blocked by insular cortex injection of Tyrosine Kinase receptor B agonist cyclotraxin‐B (p < 0.01) without affecting anxiety levels. Our study reveals that the functional activity of the brain associated with corneal neuropathic pain and neuroinflammation in the insular cortex might contribute to dry eye‐related corneal neuropathic pain.

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The medial septum (MS) contributes in pain processing and regulation, especially concerning persistent nociception. However, the role of MS glutamatergic neurons in pain and the underlying neural circuit mechanisms in pain remain poorly understood. In this study, chronic constrictive injury of the sciatic nerve (CCI) surgery was performed to induce thermal and mechanical hyperalgesia in mice. The chemogenetic activation of MS glutamatergic neurons decreased pain thresholds in naïve mice. In contrast, inhibition or ablation of these neurons has improved nociception thresholds in naïve mice and relieved thermal and mechanical hyperalgesia in CCI mice. Anterograde viral tracing revealed that MS glutamatergic neurons had projections to the lateral hypothalamus (LH) and supramammillary nucleus (SuM). We further demonstrated that MS glutamatergic neurons regulate pain thresholds by projecting to LH but not SuM, because the inhibition of MS-LH glutamatergic projections suppressed pain thresholds in CCI and naïve mice, yet, optogenetic activation or inhibition of MS-SuM glutamatergic projections had no effect on pain thresholds in naïve mice. In conclusion, our results reveal that MS glutamatergic neurons play a significant role in regulating pain perception and decipher that MS glutamatergic neurons modulate nociception via projections to LH.